American Journal of Clinical Nutrition, Vol 27, 1369-1379, Copyright © 1974 by The American Society for Clinical Nutrition, Inc.

Bile acid metabolism and hepatic disease following small bowel bypass for obesity

¹ From the Divisions of Gastroenterology and Endocrinology and Metabolism in the Department of Medicine, the Department of Pediatric Surgery, and the Department of Pharmacology and Experimental Therapeutics, the Johns Hopkins University School of Medicine, Baltimore, and the Biochemistry Research Division, Sinai Hospital of Baltimore, Baltimore, Maryland

A possible relationship of altered bile acid metabolism to liver disease following jejunoileal bypass for morbid obesity was investigated in five patients. Four months postoperatively, there was impaired liver function, significant hepatic steatosis and, in one patient, the appearance of stellate fibrosis. The relative percentages of bile acids in bile were unaltered by surgery, but in three patients there was a postoperative increase in the ratio of glycine to taurine bile acid conjugates. These latter changes could not be explained by a taurine deficiency since plasma taurine levels remained unchanged. In four patients there was a marked elevation in serum bile acids postoperatively, predominantly in cholic acid and chenodeoxycholic acid. In the one patient who developed progressive fibrosis, serum cholic acid was increased 192-fold, chenodeoxycholic acid 195-fold and lithocholic acid, a well-known hepatotoxin, 14-fold. However, biliary lithocholic acid in this patient was entirely in the water-soluble and presumably rapidly excretable sulfated form. Analysis of bile acids in this patient's liver revealed an absence of lithocholic acid and an elevation in chenodeoxycholic acid to levels known to cause hepatic injury. From these studies it appears that altered bile acid metabolism is not the sole factor responsible for all of the hepatic changes following surgery. It is proposed, however, that increased levels of chenodeoxycholic acid in association with protein malnutrition may be responsible for postoperative hepatic fibrosis.